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Medicine Year 1 - Semester 2 - Part 2 > Overview of Cancer Chemotherapy > Flashcards

Overview of Cancer Chemotherapy Flashcards

1
Q

What is cancer ?

A

Neoplasia - new growth

Uncontrolled proliferation of abnormal forms of the body’s own cells.

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2
Q

Characteristics of cancer cells

A
  1. Uncontrolled proliferation
  2. Invasiveness
  3. Metastases
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3
Q

State the 2 main causes of cancer

A

Mutations in DNA resulting in production of altered cells which have changes in proliferating mechanisms.

OR

Changes in the DNA caused by covalent modification.

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4
Q

Changes in the DNA caused by covalent modification

A

Spontaneous or genetic predisposition

Ionising Radiation or UV radiation

Chemical Carcinogens

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5
Q

Key feature of cancer

A

Cancer is a multi-step process

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6
Q

State the 3 main approaches to dealing withe established cancers

A

Surgical excision
Radiotherapy
Chemotherapy

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7
Q

Immune response

A

Good anti-microbial
Poor anti-cancer

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8
Q

Body defences response

A

Good anti-microbial
Poor anti-cancer

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9
Q

Mechanism of action of alkylating agents

A

Alkylation of the 7 nitrogen - destabilises the IMIDAZOLE ring.

Opening of the IMIDAZOLE ring

Depurination-excision of guanine residues and repair of DNA - opportunity for mutation

This resulting damage to DNA by alkylating agents triggers cell death by apoptosis.

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10
Q

State the 4 types of traditional agents (cancer chemotherapies)

A

Alkylating agents
Antimetabolites
Cytotoxic antibiotics
Plant derivatives

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11
Q

Describe Alkylating agents

A

Most commonly employed anti-cancer drugs.

Bind DNA in cancer cells, causing cell death.

Intra-strand cross-linking of DNA.

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12
Q

What are alkylating agents capable of doing ?

A

Forming covalent bonds with suitable nucleophilic substances in the cell under physiological conditions.

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13
Q

Describe guanine residues in DNA

A

Normally guanine residues in DNA exist predominantly in the keto tautomer.

This allows them to form base pairs with cytosine.

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14
Q

Describe alkylation of guanine

A

When the 7position nitrogen of guanine is alkylated it becomes more acidic and the keto turns into enos.

This modified guanine can mispair with thymine residues in DNA synthesis.

This creates a mutation.

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15
Q

Example of Nitrogen mustards

A

Cyclophosphamide

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15
Q

State the 6 major classes of alkylating agents

A

Nitrogen mustards
Ethylenimines
Alkylsulphonates
Hydrazines and Traizines
Nitrosoureas
Platinum based compounds

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16
Q

Example of Ethylenimines

A

Thiotepa

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17
Q

Example of Alkylsulphonates

A

Busulphan

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18
Q

Example of Hydrazines and Traizines

A

Temozolomide

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19
Q

Example of Nitrosoureas

A

Lomustine, Carmustine

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20
Q

Example of Platinum based compounds

A

Cisplatin

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21
Q

Describe the action of nitrogen mustards - e.g. cyclophosphamide

A

Cyclophosphamide activated in the liver by P450 mixed function oxidases.

Involved in cross-linking of DNA

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22
Q

Describe the action of alkylsuphonates - e.g. busulphan

A

Busulphan has a selective effect on the bone marrow.

Used in chronic granulocytic leukaemia.

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22
Q

Busulphan

A

Selective effect on the bone marrow, depressing the formation of granulocytes and platelets in low dosage and red cells in high dosage.

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23
Describe the action of platinum based compounds - e.g. cisplatin
Action is analogous to that of the alkylating agents. Binds DNA - causes intrastrand cross-links Used for ovarian cancer
23
Describe the action of nitrosoureas - e.g. lomustine, carmustine
These drugs are LIPID soluble and can therefore cross the blood-brain barrier. May be used against tumours of the brain and meninges.
24
State the major groups of anti-metabolites
Antifolates Antipyramidines Antipurines
25
Example of an antifolate
Methotrexate
26
Example of an antipyramidine
5-FU Gemcitabine
27
Example of an antipurine
Mercatopurine Thioguanine
28
Describe antifolate - methotrexate
Folate analogue - usually given orally - low lipid solubility, so doesn't cross blood brain barrier easily - polyglutamated which means it can be retained within cells for weeks
29
Key feature of antifolates - methotrexate
Polyglutamated which means it can be retained within cells for weeks
30
Describe antipyramidines - fluorouracil 5-FU
Fluorouracil interferes with thymidylate synthesis (DTMP) It is converted into FDUMP - fraudulent nucleotide This inhibits DNA polymerase.
31
Action of fludarabine
Antipurine - Fludarabine in its triphosphate form inhibits DNA polymerase
32
Function of cytotoxic antibiotics
Anti-tumour antibiotics produce their effects mainly by direct action on DNA.
33
Give some classes of cytotoxic antibiotics
Anthracyclines Dactinomycin Bleomycin Mitomycin
34
Example of anthracyclines
Doxorubicin
35
Mechanism of action of doxorubicin
It binds to DNA and inhibits both DNA and RNA synthesis. Main cytotoxic effect appears to be mediated through an effect on topoisomerase 2 - the activity of which is markedly increased in proliferating cells.
36
Action of doxorubicin on DNA-topoisomerase II
Doxorubicin intercalates into DNA and blocks the DNA-topoisomerase II complex.
37
Dactinomycin action
Interfering with the movement of RNA polymerase along the gene - preventing transcription.
38
Bleomycins action
Degrade preformed DNA, causing chain fragmentation and release of free bases.
38
Mitomycin action
After enzymatic activation in cells, functions as a bifunctional alkylating agent. Cross-links DNA and may degrade DNA through generation of free radicals.
39
Plant derivatives functions
Spindle poisons - affect microtubule function and prevent mitotic spindle formation Vinca Alkaloids & Taxanes: inhibit MT function Captothecins & Etoposide: inhibit RNA synthesis and topoisomerase 2
40
Common plant derivatives
Vinca alkaloids Taxanes Camptothecins Etoposide
41
Function of vinca alkaloids
Binds tubules and prevents polymerisation into microtubules
42
Function of taxanes
Stabilises (freezes) microtubules
43
Function of camptothecins
Binds to and inhibits topoisomerase I
44
Function of etoposide
Inhibits mitochondrial function, nucleoside transport and topoisomerase II.
45
Example of vinca alkaloids
Vincristine Vinblastine
46
Example of taxanes
Paclitaxcel Docetaxel
47
Example of Camptothecins
Irinotecan
48
State some other anti-cancer drugs
Hormones (hormone inhibitors) Monoclonal antibodies Protein kinase inhibitors Miscellaneous agents
49
Drawbacks of chemotherapy of cancer
Target cell proliferation NOT the more lethal properties of invasiveness and metastases. Non-specific cell killers rather than being aimed at the particular changes which make a cell malignant. The development of resistance to anti-cancer drugs. Leaves some remaining cells
50
Describe the side-effects caused by chemotherapy
Side effects relate to body systems: Healthy cells which have a high rate of growth and multiplication include cells of bone marrow, hair, GI mucosa and skin.
51
When do side effects of cancer chemotherapy occur ?
7-14 days post cancer treatment. This can be cumulative over many cycles.
52
KEY drawback of chemotherapy
Patient compliance due to side-effects Not competing the therapy regimen.
53
Tumour Lysis Syndrome
Acute side-effect and a metabolic emergency. Occurs due to rapid cell lysis and large amounts of cell metabolites in blood. Characterised by hyper: - Uricaemia - Phosphataemia - Kalaemia Hypocalcaemia
54
If tumour lysis syndrome is left untreated what can it cause ?
Acute renal failure Cardiac arrest Death
55
State some specific side effects to systems of chemo
Bone Marrow Gastro-intestinal Mucositis
56
Fatigue
Often multi-factorial, treat cause if known, involves physio/occupational therapists in care.
57
Body image side effects
Hair loss Weight gain/loss Appearance of intervention wounds
58
Altered renal function
Care with drug choices, dose and frequency
58
Peripheral neuropathy
Counsel patient about the need for care if injured, consider analgesia for nerve pain.
59
Delayed effects of chemo
Infertility Secondary Malignancy
60
Key action of methotrexate
Inhibits: - purine synthesis - DTMP synthesis
61
Key action of 5-fluorouracil
Inhibits DTMP synthesis
62
Key action of alkylating agents
Cross-links DNA
63
Key action of doxorubicin, etoposide, amasacrine, campothecins
Inhibit: - topoisomerase II - RNA synthesis
64
Key action of dacintomycin
Intercalates in DNA Inhibits: - Topoisomerase II - RNA synthesis
65
Key action of Vinca Alkaloids, Taxanes
Inhibits function of microtubules
66
Key action of cytarabine
Inhibits: - DNA polymerase - RNA function

Medicine Year 1 - Semester 2 - Part 2 (53 decks)

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